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小分子干扰RNA介导的3T3-L1细胞中醛氧化酶1的敲低会损害脂肪生成和脂联素释放。

Small-interference RNA-mediated knock-down of aldehyde oxidase 1 in 3T3-L1 cells impairs adipogenesis and adiponectin release.

作者信息

Weigert Johanna, Neumeier Markus, Bauer Sabrina, Mages Wolfgang, Schnitzbauer Andreas A, Obed Aiman, Gröschl Benedikt, Hartmann Arndt, Schäffler Andreas, Aslanidis Charalampos, Schölmerich Jürgen, Buechler Christa

机构信息

Department of Internal Medicine I, Regensburg University Hospital, Regensburg, Germany.

出版信息

FEBS Lett. 2008 Aug 20;582(19):2965-72. doi: 10.1016/j.febslet.2008.07.034. Epub 2008 Jul 29.

Abstract

Aldehyde oxidase 1 (AOX1) is highly abundant in the liver and oxidizes aldehydes thereby generating reactive oxygen species. Enzymes involved in detoxification of aldehydes are expressed in adipocytes and alter adipogenesis, therefore the functional role of AOX1 in adipocytes was analyzed. AOX1 mRNA was higher in visceral compared to subcutaneous human adipose tissue but AOX1 protein was detected in both fat depots. AOX1 expression in adipocytes was confirmed by immunohistochemistry and immunoblot. AOX1 was induced during adipocytic differentiation and was downregulated by fenofibrate in differentiated cells. Knock-down of AOX1 in preadipocytes led to impaired lipid storage and adiponectin release in the differentiated cells. These data indicate that AOX1 is essential for adipogenesis and may link energy and drug metabolism.

摘要

醛氧化酶1(AOX1)在肝脏中高度丰富,可氧化醛类从而产生活性氧。参与醛解毒的酶在脂肪细胞中表达并改变脂肪生成,因此分析了AOX1在脂肪细胞中的功能作用。与皮下人类脂肪组织相比,内脏脂肪组织中AOX1 mRNA水平更高,但在两个脂肪库中均检测到AOX1蛋白。通过免疫组织化学和免疫印迹证实了AOX1在脂肪细胞中的表达。在脂肪细胞分化过程中AOX1被诱导,在分化细胞中被非诺贝特下调。前脂肪细胞中AOX1的敲低导致分化细胞中脂质储存和脂联素释放受损。这些数据表明AOX1对脂肪生成至关重要,可能将能量代谢与药物代谢联系起来。

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